Intracranial Space occupying lesions

1. SPACE OCCUPYING
LESIONS
OF THE BRAIN
16 DECEMBER 2013

2. CONTENT
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DEFINITION OF SOL
TYPES OF SOL IN THE BRAIN
SIGNS AND SYMPTOMS
NEUROIMAGING AND OTHER
INVESTIGATIONS
TREATMENT
PROGNOSIS

3. DEFINITION OF SOL


Substantial physical lesions, e.g. neoplasm,
hemorrhage, granuloma, which occupy space;
the effect is more significant if the lesion is
within a space confined by bone, e.g. thorax,
cranium, bone marrow cavity.
SOL OF THE BRAIN : Within the cranium or
skull.

4. TYPES OF SOL IN THE
BRAIN

Neoplasm
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Infection
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Meningioma, glioma, pituitary tumour
E.g. abscess, tuberculoma
Vascular lesions
AVM, cavernoma, giant aneurysm
 Hemorrhage


5. Neoplasm

6. Infection

7. Vascular lesions

8. SIGNS AND SYMPTOMS

Neurological phenomena is caused by irritation or destruction of
brain tissue, e.g.
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Focal seizures (Jacksonian epilepsy)
Paralysis.
Headache
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Do not respond to simple medicines refers to the possibility of ICSOL.
The headache is felt in the midline over the head of at times it is referred
over the site of lesion, e.g meningioma.
It will be continuous and progressive, paroxysmal (as in migraine), or
aggravated by coughing, stooping forward and changing postures.
Patients with headaches that wake them at night or are worse in the
morning, or who have focal neurologic deficits, require urgent
neuroimaging.
However, many patients with brain tumours present with headaches that
are indistinguishable from tension headaches.

9. SIGNS AND SYMPTOMS
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Vomiting and visual loss:
 In many cases, protracted vomiting is a common symptom.
 Projectile vomiting is mistaken for gastrointestinal or
psychiatric disturbances.
 Failure of vision because of late papilloedema phenomenon.
Impairment of conscious level due to raised intracranial pressure.
 Headaches, nausea, vomiting, and changes in mental status,
cognition, and progressive altered levels of consciousness
alongside other indicative signs such as papilloedema usually
reflect raised intracranial pressure from mass effect or
hydrocephalus.
Late onset of seizures:
 Any type of seizure if occurs for the first time after the age of
15 years will suggest the possibility of ICSOL.

10. SIGNS AND SYMPTOMS


Both nonspecific and focal neurologic complaints and symptoms
can alert the primary care physician or neurologist to the
possibility of an underlying mass lesion and indicate the need for
further work - up.
Key aspects of the history that help differentiate neoplastic
lesions from other diagnoses include
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Timing of symptom onset,
Tempo of progression,
Severity of symptoms.
Systemic symptoms and the presence of other diseases or
hereditary syndromes are additional valuable pieces of
information that can help narrow the diagnosis by their
association with specific CNS tumours.

11. SIGNS AND SYMPTOMS
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Other symptoms and signs, such as global mental status changes,
are quite common and include apathy, change in personality,
irritability, psychomotor retardation, lethargy, and forgetfulness.
Such nonspecific impairments in mental function have been
linked to lesions in the frontal and temporal lobes, corpus
callosum, thalamocortical fibers, and reticular formation, among
others.
Still other non-localizable presentations are the result of
multifocal tumours, often seen in metastatic disease, presenting
with a mixture of focal signs and symptoms that can be confused
for generalized clinical manifestations.

12. SIGNS AND SYMPTOMS

Brain tumour
 Symptoms produced by brain tumors may be either
nonspecific or focal, and in general tend to be subacute in
onset.
 The presentation varies widely and neither a normal
neurologic exam nor presentation with acute onset of
symptoms rules out a brain tumour.
 At the outset many brain tumours produce minimal or no
symptoms.
 Brain tumors can also present with acute onset stroke - like
symptoms.

13. SIGNS AND SYMPTOMS

Brain tumour
 This type of acute presentation is usually the result of a focal
seizure or hemorrhage into the tumour bed.
 The rate of progression of symptoms is also quite variable
but tends to be gradual over weeks to months, helping to
differentiate neoplasms from other more static disorders such
as degenerative disease or more rapidly progressing infectious
conditions.
 By paralleling the growth and spread of CNS neoplasms, the
rate of symptomatic progression can serve as a rough clinical
estimate to tumour grade.

14. SIGNS AND SYMPTOMS

Brain tumour
 Typically, benign tumours such as meningiomas, or low grade neoplasms such as oligodendrogliomas, will have a
slower progression of symptoms than more malignant
tumours such as glioblastomas.
 A careful review of systems, for instance, should identify
symptoms such as weight loss, lethargy, and night sweats that
are nonspecific but can be associated with many types of
cancers.
 When combined with neurologic symptoms, these symptoms
should raise suspicion of primary or metastatic CNS
neoplasms, though should not rule out subacute infectious,
inflammatory, or autoimmune CNS processes.

15. SIGNS AND SYMPTOMS

Brain tumour
 Likewise, a detailed review of past medical history may
identify genetic syndromes or other conditions with a higher
than normal incidence of CNS neoplasms.
 Neurofibromatosis type 1 is associated with gliomas and
cutaneous manifestations,
 Neurofibromatosis type 2 is associated with vestibular
schwannomas and meningiomas,
 Von Hippel – Lindau syndrome is associated with
hemangioblastomas.

17. SIGNS AND SYMPTOMS

Intracranial Infection
 The onset of acute bacterial meningitis is rapid: hours to a
day or so.
 Classic clinical findings include signs of an acute cerebral
disorder, with lethargy, seizures, and agitation as well as
specific signs of meningeal involvement manifested by severe
neck stiffness, called meningismus
 Fever that may not be immediately present.
 The patient rapidly becomes confused, sleepy, obtunded, and
often comatose

18. SIGNS AND SYMPTOMS

Intracranial Infection
 For identifying the presence of inflamed meningeal coverings
involving the lumbosacral nerve roots:
 The Kernig sign
 is elicited by flexing the patient’s hip to a 90-degree
angle and then attempting to passively straighten the
leg at the knee; pain and tightness in the hamstring
muscles prevent completion of this maneuver. This
sign should be present bilaterally to support a
diagnosis of meningitis.
 The Brudzinski sign
 is positive if the patient’s hips and knees flex
automatically when the examiner flexes the patient’s
neck while the patient is supine.

21. SIGNS AND SYMPTOMS

Brain abscess
 The cardinal symptom of brain abscess is persistent and
progressive headache, usually followed by focal neurologic
manifestations.
 Only two thirds of patients have fever.
 Papilloedema and other signs of increased intracranial
pressure may occasionally develop; however, the availability
of imaging studies makes it more likely that the abscess will
be identified prior to its obtaining significant enough mass to
create increased intracranial pressure.

22. SIGNS AND SYMPTOMS

Subdural abscess
 It is typically characterized by a purulent collection within the
potential space between the dura mater and arachnoid
membrane
 Localized swelling, erythema, headache, or tenderness of the
site overlying the primary infection may occur.
 As the illness progresses, the headache becomes generalized
and severe, with a high fever, vomiting, and nuchal rigidity
developing.
 Seizures, hemiparesis, visual field defects, and papilledema
sometimes occur.

23. SIGNS AND SYMPTOMS

Intracranial Hemorrhage
 Intraparenchymal hemorrhages vary in presentation
depending on the site of the bleeding.
 In approximately 60% of patients, neurologic symptoms
develop gradually or stepwise over a period of hours.
 To some extent, the location and size of the hematoma
predict clinical outcome.
 Headache occurs at presentation in approximately 40% of
patients with ICH.
 Less commonly, headache develops within a few days after
the ictus.
 Intracerebral hemorrhages presenting with headache are
often located at the brain surface or within the cerebellum.

24. SIGNS AND SYMPTOMS

Intracranial Hemorrhage
 Depression in the level of consciousness and vomiting occur
in 50% of patients, particularly those with large cerebellar
bleeds.
 Seizures occur at onset in up to 10% and are seen most
commonly with lobar bleeds in the anterior circulation.
 There are rare incidences of patients with deep hemorrhages
having seizures.

25. SIGNS AND SYMPTOMS

Intracranial Hemorrhage
 The subsequent risk for seizures in ICH patients is up to 29%
for those with lobar hemorrhages but only 4% for those with
deep hemorrhages.
 Other symptoms seen in association with ICH include lowgrade fever without obvious infection, cardiac arrhythmias,
and dysautonomia, especially with pontine bleeds.

31. NEUROIMAGING AND
OTHER INVESTIGATIONS
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Routine blood tests will include FBC, U&E and LFTs.
Na+ will be low due to inappropriate ADH secretion.
Skull x-ray is usually done , but if pineal gland is calcified, then a
shift is seen.
Imaging studies include CT scan and MRI-scan are required.
Both works very good but MRI is better in delineating soft
tissue.
A known primary tumour will exist or it can be sought out by
chest x-ray or by mammography.
Imaging tests will indicate the site of a lesion but usually it will
not indicate the nature or whether it is a tumour or an abscess.

32. NEUROIMAGING

Skull radiograph
 Pituitary fossa abnormalities.
 Bone density changes (e.g. tumour, meningioma, Paget’s).
 Position of calcified pineal

33. NEUROIMAGING

Cranial CT
 Disturbances in the normal anatomy of the ventricular
system.
 Skull base and vault.
 Width of cortical fissures/sulci.
 Midline shift.
 Areas of abnormal tissue density.
 Opacity or lucency of sinuses.
 Normal flow voids.

34. NEUROIMAGING

Cranial CT
 High density (‘white’) signal
 Fresh blood.
 Calcification:
 Slow growing tumour.
 AVM/aneurysm.
 Hamartoma.
 In pineal/choroid plexus/basal ganglia, may be
normal.

35. NEUROIMAGING

Cranial CT
 Low density (‘black’) signal
 Infarction.
 Tumour.
 Abscess.
 Oedema.
 Encephalitis.
 Resolving haematoma.

36. NEUROIMAGING

Cranial CT
 Mixed density
 Tumour.
 Abscess.
 AVM.
 Contusion.
 Haemorrhagic infarct.

37. NEUROIMAGING

Cranial CT (After administration of IV contrast medium)
 Common patterns of enhancement include
 Ring enhancement of tumours and abscesses.
 Solid enhancement of meningiomas.
 Meningeal enhancement with meningeal disease
involvement.

38. NEUROIMAGING

Magnetic resonance imaging (MRI)
 In general
 T1 CSF is hypointense (‘black’); fat and mature blood clot
white.
 T2 CSF is hyperintense (‘white’).
 MRI with enhancement (Intravenously administered
gadolinium leaks through areas of damaged blood--brain
barrier to give a marked enhancement)
 Ischaemia.
 Infection.
 Tumour (may help differentiate from surrounding
oedema).
 Active demyelination.

40. NEUROIMAGING

Positron Emission Tomography
 Form of molecular imaging that requires an injection of a
radioactive tracer into the blood stream.
 Radionuclide tracers are prepared using a cyclotron device
and a wide variety of molecules can be labelled by this means,
including metabolically active substances.
 18 F-fluorodeoxyglucose (FDG).

41. NEUROIMAGING

Positron Emission Tomography
 Metabolic imaging technique that is capable of differentiating
benign and malignant tumours more accurately.
 Used extensively in staging of brain tumours as it can
produce a visual mapping of biochemical changes caused by
the metabolic activity of the brain tumour.

42. Patient with a high grade Glioma tumour showing
(a) T1w post contrast enhancing margins with the central area of necrosis in
the tumour,
(b) T2w image confirming the findings.
(c) The combined PET-CT using FET tracer shows the tumour clearly with
infiltrations to the cerebral cortex and infiltration to the contralateral
hemisphere.

43. NEUROIMAGING

Angiography
 Strongly suspected or confirmed SAH.
 Suspected cerebral vasculitis
 Delineation of other vascular abnormalities
 arteriovenous malformations, AVM
 Delineation of tumour blood supply

44. NEUROIMAGING

45. NEUROIMAGING

46. NEUROIMAGING

47. NEUROIMAGING

48. NEUROIMAGING

50. INVESTIGATIONS

Lumbar puncture (LP)
 CNS Infection:
 Meningitis.
 Encephalitis/ Cerebral abscess
 Suspected subarachnoid haemorrhage (SAH).
 In general, a –ve CT does not exclude a SAH.
 Suspected malignancy with meningeal involvement.
 To seek specific antibodies/markers in CSF,
 Syphilis.
 Tumour markers.

51. INVESTIGATIONS

Diagnostic & prognostic antibodies and other markers in
blood
 Systemic infections
 Serology for many diseases

PCR for TB.
Disorders of coagulation: thrombophilia screen currently commonly
 Protein S and C levels.
 Antithrombin III levels.
 Screening for the Leiden mutation in factor V.
 Lupus anticoagulant.


e.g. Borrelia in Lyme disease; HIV.

52. INVESTIGATIONS

Diagnostic & prognostic antibodies and other markers in
blood
 Tumour markers
 CEA for gut neoplasia (brain metastasis)
 Beta HCG, Alphafetoprotein in pineal tumour
 Endocrinopathies
 TSH, T4, GH, Prolactin, Cortisol in pituitary lesion

53. INVESTIGATIONS


Neuro-otology
 Pure tone audiometry
 For lesion with the involvement of auditory meatus
 Acoustic neuroma
 CPA meningioma
Neuro-ophtalmology
 Visual field and Visual acuity
 Lesion with the involvement of optic nerves, optic tract,
optic radiation and visual cortex

54. TREATMENT
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Management will depends mainly on the cause of lesion.
If possible, especially with primary tumours complete excision is
done but this is so difficult due to infiltration and by surrounding
structures.
These will vary with radiosensitivity and will show response to
chemotherapy.
If malignancy is metastatic then treatment should include
radiotherapy.
However, surgery is contemplated with up to 3 metastases.
Haematoma will need evacuation.
Infectious lesions will need both evacuation and antibiotics.

55. TREATMENT
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Other treatments are required either as a part of radical treatment
or as palliative care.
Dexamethasone will reduce cerebral oedema.
Mannitol will reduce raised intracranial pressure.
Anticonvulsants are required but are not to be given
prophylactically .
Treat headache with codeine phosphate because it will avoids the
pupillary effect of opiates.

56. TREATMENT

Biopsies
 A biopsy should be undertaken to answer specific questions,
in the light of a differential diagnosis formulated following
history, examination and other investigations.
 Diagnosis and management of suspected primary and
some metastatic brain tumours. (Tissue diagnosis)
 Differential diagnosis of other mass lesions (inflammatory
and infective).
 Differentiation of radiation necrosis and tumour regrowth.
 Differentiation of neoplastic and non-neoplastic cysts (and
their drainage).
 Diagnostic biopsy of a suspected infectious lesion that has
not responded to a trial of therapy.
 Diagnosis of cerebral vasculitis or vasculopathy.

57. TREATMENT

Surgery
 Cytoreduction
 Cytoreductive surgery for low - grade and malignant
gliomas improves survival.
 Survival benefits for the resection of single and multiple
brain metastases.
 Extent of resection (EOR) may be significant in
determining survival for both low – grade and high grade gliomas.

58. TREATMENT

Surgery
 Surgical Cure
 Many extra - axial tumors and some intra - axial tumors
afford the neurosurgeon the opportunity for gross total
resection and surgical cure.
 Benign tumors such as meningiomas, pituitary adenomas,
cranial nerve schwannomas, chordomas, dermoids and
epidermoids, choroid plexus papillomas, pilocytic
astrocytomas, and hemangioblastomas may, in many
cases, be cured with complete surgical resection.

59. TREATMENT

CNS Infection
 Antibiotic treatment must be initiated as soon as possible,
and later guided by CSF examination results.
 Patients must receive at least 10 days of high-dose IV
antibiotics that easily cross the blood–brain barrier.
 Empiric IV therapy with a third-generation cephalosporin,
such as ceftriaxone or cefotaxime, plus vancomycin must
commence pending results of the bacterial cultures.
 High-dose corticosteroids, administered before antibiotic
therapy, are recommended for all children and should be
seriously considered for adults with community-acquired
meningitis.
 When culture and sensitivity data are available, a specific
antimicrobial therapy can be determined.

60. TREATMENT

Brain abscesses
 Empiric medical therapy is started with a third- or fourthgeneration cephalosporin or penicillin plus metronidazole,
depending on the setting.
 Brain edema associated with acute brain abscess necessitates
use of steroids and mannitol, as well as phenytoin, to prevent
convulsions.
 Patients must receive at least 4 to 6 weeks of high-dose IV
antibiotics that easily cross the blood–brain barrier, followed
by 2-4 weeks of oral antibiotics.

61. TREATMENT

Brain abscesses
 Therapeutically, the abscess may be directly aspirated.
 Burrhole and drainage of abscess or craniotomy and excision
of abscess may be indicated depending on the size of the
abscesses and the depth from the cortical surface.
 Surgery may not be necessary if follow-up CT demonstrates
decreased abscess size.

62. TREATMENT

Cerebral tuberculoma
 PCR and CSF culture or culture of biopsied lesional material
confirms the diagnosis.
 Because standard medical therapy is usually successful if
multidrug resistance is not identified, antituberculous therapy
must be attempted before surgery is contemplated.
 Of course, if there are signs of impending herniation,
immediate surgery is indicated.

63. TREATMENT

Intracranial Hemorrhage
 The initial management of ICH, after ensuring adequate
ventilation and hemodynamic stability, involves correcting
coagulopathies, treating hypertension, and addressing the
possibility of increased intracranial pressure.
 In
patients with intraventricular blood and early
hydrocephalus, placement of a temporary external drain
should be considered.
 Beyond these basics principles, the best treatment of ICH
remains unclear and quite variable from center to center and
in different countries.
 Although some advocate invasive techniques for hematoma
evacuation, others rely mostly on medical treatment and
supportive care

64. TREATMENT

Intracranial Hemorrhage
 However, when a nondominant hemispheric or cerebellar
ICH threatens impending herniation and before the patient’s
level of consciousness significantly deteriorates, emergent
surgery may be lifesaving and may provide a reasonably good
recovery, especially in younger patients.

65. PROGNOSIS

Intracranial Neoplasm
 Gliomas are rarely completely excised, as infiltration spreads
beyond the radiologically evident boundaries of the tumour.
 Recurrence is therefore common, even if the tumour mass is
apparently completely removed.
 Prognosis for benign tumours is good, provided complete
surgical excision can be achieved.

66. PROGNOSIS

Intracranial Infection
 Of patients with bacterial meningitis, approximately 15%
experience acute and chronic complications, including various
cranial nerve dysfunction, particularly those affecting
extraocular function (cranial nerves III, IV, and VI), CN-VII,
and sometimes CN-VIII, although this is less common today
with the antibiotics lacking specific ototoxicity or vestibular
toxicity.
 Even with early diagnosis, mortality rates are still at least 10%
for meningococcal and 30% for pneumococcal meningitis.

67. PROGNOSIS

Intracerebral hemorrhage
 Surgery demonstrated slightly better outcome (26.1% vs.
23.8%), but survival rates appeared to be similar in surgically
and medically treated patients.
 The outcome from surgery likely depends on several factors,
including the fact that deep-seated basal ganglia or thalamic
hemorrhages are difficult to evacuate without disrupting
surrounding normal structures and exacerbating brain
damage, especially with open craniotomy.
 Patients who have small hematomas (smaller than 30 cm3)
seem to do generally well without surgical evacuation.
However, larger hematomas (larger than 60 cm3) do poorly,
even when evacuated surgically.

68. THANK YOU